🔹Lymphatic aging represented by cellular and functional changes is an increased risk factor for geriatric disorders.
🔹Advanced age and organ deterioration are crosslinked with the progression of some lymphatic-associated diseases.
🔹Lymphangiogenesis and lymphatic remodeling are involved in the regulation of aging-related pathological processes.
🔹Targeting aging-induced lymphatic dysfunction will facilitate the development of interventions to reduce the burden of age-related diseases.
🔹Promotion of lymphangiogenesis is beneficial to inflammation regression, edema resolution and wound healing via the delivery of immune cells or inflammatory mediators.
🔹In aged mouse recipient, a better transplantation outcome is explained due to lower lymphangiogenic potency.
🔹Lymphangiogenesis has a pivotal role in the progression of lymphatic-associated diseases, which represents a hallmark of inflammatory responses via the regulation of pro-inflammatory cytokines, e.g., IL-1β, IL-6, and TNF-α, and lymphangiogenic factors, e.g., VEGF-C/-D.
🔹The macrophages, a well-known source of VEGF-A/-C/-D and multiple cytokines, actively participate in inducing lymphangiogenesis in the inflamed and wounded skin.
🔹Decreased macrophage number and activation lead to reduced lymphangiogenesis and contribute to impaired diabetic wound healing, due to persistent edema and delayed removal of debris and inflammatory cells.
🔹In old age, low-grade inflammation is a central driver of aging-related impairment and disease, whereas multiple factors, such as increased TNF-α and IL-6 may contribute to aging-related inflammation.
🔹Some pro-inflammatory interleukins (IL-1α, IL-1β, IL-6, IL-8) have been implicated as established SASP factors in cell-autonomous regulation of senescence and stimulation of proliferation, suggesting that aging and inflammation are two closely linked processes.
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